Your Heart Rate Should Slow During Sleep

By: Robert W. Griffith, MD

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Normally, the heart rate slows during sleep at night; this is called the nocturnal 'dip'. In a study from Israel, ambulatory monitoring was used to study the normal sleeping dip in heart rate in relation to mortality ...

Summary

Ambulatory monitoring was used to establish that absence of the normal sleeping 'dip' in heart rate is associated with increased all-cause mortality.

Introduction

In the old days, the first thing the doctor did when making a house call was to take the pulse. Medical students were taught the different adjectives to use in describing the pulse: full pulse, round pulse, bouncing pulse, strong pulse, irregular, soft, compressible, weak, fluttering, and so on. And if you determined that the pulse was irregular, you had to estimate if it was regularly irregular or irregularly irregular. All this has been superseded by ECG tracings, and examining the pulse has lost some of its diagnostic magic. But Israeli physicians have recently examined the resting heart rate for its use in predicting cardiovascular and non-cardiovascular events. In particular, they studied the heart rate during sleep; in normal subjects, the heart rate dips during sleep by at least 10%. The findings from this study are reported in the Archives of Internal Medicine .

What was done

Ambulatory blood pressure monitoring (ABPM) was used to obtain 24-hour records of heart rate during daily activity and nighttime sleep. A group of nearly 4,000 patients who had been referred for ABPM over a 14-year period provided the records for analysis. Their average age was 55, with 53% of them being women; over half the patients were being treated for high blood pressure.

Baseline data collected included height, weight, and information on treatments taken for high blood pressure and diabetes. The participants were asked to keep a sleep diary, including daytime naps, recording actual periods of sleep.

The 24-hour ABPM was obtained from a Spacelabs monitor applied between 8:00 and 10:00 am, and removed 24 hours later. Blood pressure was measured by a mercury sphygmomanometer. Heart rates were measured at the same time as blood pressure. Recordings were made every 20 minutes during the day and every 30 minutes during the night.

For the purpose of this study, average awake and average sleep heart rates were used to identify "non-dipper" patients. This was defined as follows: (awake value minus sleep value)/awake value is less than 0.1. In other words, the sleep dip was less than 10%.

Analysis of the association between mortality and heart rates was done by categorizing participants into one of 10 classes (or deciles) according to their heart rate variables (awake rate, sleep rate, and %age heart rate dip).

The "outcome measure" was overall or all-cause mortality; information on the death of subjects was obtained from the National Population Register, using the individual national identification number.

What was found

The average body mass index (BMI) of the participants was 27.2 - i.e. they were overweight but not obese. Diabetes was present in 9%, hypertension in 58%, and 31% said they took daytime naps. The average follow-up period was 7 years. During the study there were 303 deaths, resulting in an overall mortality rate of 10.9 per 1,000 patient-years.

Average heart rates were, in general, higher in women, those with a higher BMI, and in treated diabetics. Increasing age and treated high blood pressure were associated with lower heart rates. A reduced dip in sleep heart rates was seen in the participants with these variables (i.e. women, high BMI, etc). There was no heart rate dipping during napping in those who indulged in this. And the use of beta-blocking drugs, known to influence heart rate, had no association with dipping or non-dipping.

Mortality hazard ratios (the odds of a subject dying) were calculated for each decile of the heart rate variables. The awake heart rates showed no influence on the mortality hazard ratios. With the sleep heart rates there was a slight increase in the hazard ratios with increasing decile.

However, with the heart rate dip during sleep there was a highly significant relationship between the hazard ratios and the dip deciles; the lowest decile (representing the 10% of participants with the smallest dip, having less than 3 beats a minute fall) had a hazard ratio 2.67 times that of the 10% of participants with the greatest dip during sleep. In other words, persons with the smallest dip in heart rate during sleep were over 2½ -times as likely to die in the next 7 years as those with a large night-time dip. Those exhibiting no dip at all had a mortality hazards ratio of 1.45, compared with all the "dippers".

Conclusions

Heart rate measurements during sleep can provide useful prognostic information regarding all-cause mortality. Those with very small or no dips in sleeping heart rate were about 2½ times as likely to die in the next 7 years as those with normal or large dips during sleep.

The authors of the study suggest that overactivity of the sympathetic nervous system (responsible for the 'fight or flight' type of response to alarming stimuli) is more likely to be seen in an elevated sleeping heart rate than by the awake or even the 'clinic' heart rate. Physical activity and the 'white coat effect' can influence the awake and the clinic rates, but the sleeping rate is more likely to truly represent a health problem. It should be noted that this study measured all-cause mortality, not cardiovascular mortality. The association between overall heart rates and age, BMI, and hypertension would suggest that cardiovascular deaths were mostly responsible, but these were not measured separately. That remains to be established in the next study.

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